imported>Chunbum Park |
imported>John Stephenson |
| (218 intermediate revisions by 8 users not shown) |
| Line 1: |
Line 1: |
| '''[[Gut-brain signalling]]''' describes the interaction between the gastrointestinal tract and the brain, and how secretion of varying hormones from different areas of the body causes appetite-enhancing and satiety signals to be sent to the brain. The hormones that have been most intensely studied are: ghrelin, obestatin, cholecystokinin (CCK), GLP-1, peptide YY (PYY) and insulin which all play major roles in appetite regulation. The vagus nerve is also a key mediator of regulation, and all of these inputs are processed by areas in the brain such as the hypothalamus and the nucleus tractus solitarii (NTS).
| | {{:{{FeaturedArticleTitle}}}} |
| | | <small> |
| ===Anorexic Signals=== | | ==Footnotes== |
| {{Image|diagram 3.jpg|center|350px|''Gut-Brain signaling Pathways'' Proteins and hormones activate brain pathways in different ways, either by eventual vagal activation or through peripheral circulation. The nucleus tractus solitarii and the arcuate nucleus are then activated. }} | | {{reflist|2}} |
| '''Cholecystokinin''' (CCK) is a peptide hormone synthesised by L-cells in the mucosal epithelium of the duodenum, and secreted in response to the presence of partly digested lipids and protein]]s. CCK inhibits gastric emptying and stimulates the release of digestive enzymes from the pancreas and bile from the gall bladder by acting at CCK-A receptors (mainly found in the periphery but also found in some areas of the CNS). Because gastric emptying is inhibited, the partly digested lipids and proteins are exposed to the digestive enzymes and bile so are further broken down. As the lipids and proteins are broken down, CCK secretion declines.
| | </small> |
| | |
| CCK acts as a ‘gatekeeper’ for the response of other gut-brain signalling hormones on the afferent vagal neurons. At low levels (after fasting), CCK stimulates the expression of receptors associated with the stimulation of food intake, including receptors for melanin concentrating hormone (MCH)-1 and cannabinoid CB1 receptors. At high levels (after food consumption), MCH-1 and CB1 receptors are down- regulated. Therefore CCK, at a high or low concentration, can affect how afferent vagal neurons respond to other neurohormones.
| |
| | |
| In rats, CCK inhibits food intake in younger individuals more effectively than in older individuals. It also has a greater effect in males than in females.
| |
| | |
| '''Glucagon-like peptide-1''' (GLP-1) is a hormone secreted from L-cells in the mucosal epithelium of the duodenum and small intestine. It is derived from the ''pro-glucagon'' gene, and is secreted into the circulation in response to the presence of nutrients. It acts at the pancreas, where it stimulates insulin secretion and suppresses glucagon secretion. It also increases insulin sensitivity. GLP-1 also activates anorexigenic neurons in the arcuate nucleus via the caudal brainstem. Activation of these neurons induces satiety and decreases food intake/hunger. It also decreases gastric emptying, so adds to the feeling of being ‘full’. At higher concentrations, GLP-1 causes nausea, and can induce conditioned taste aversion, where the brain associates the taste of a certain food with being toxic (usually after an individual consumes a food that had made them sick).
| |
| | |
| [[Gut-brain signalling|.....]]
| |
Latest revision as of 09:19, 11 September 2020
The Mathare Valley slum near Nairobi, Kenya, in 2009.
Poverty is deprivation based on lack of material resources. The concept is value-based and political. Hence its definition, causes and remedies (and the possibility of remedies) are highly contentious.[1] The word poverty may also be used figuratively to indicate a lack, instead of material goods or money, of any kind of quality, as in a poverty of imagination.
Definitions
Primary and secondary poverty
The use of the terms primary and secondary poverty dates back to Seebohm Rowntree, who conducted the second British survey to calculate the extent of poverty. This was carried out in York and was published in 1899. He defined primary poverty as having insufficient income to “obtain the minimum necessaries for the maintenance of merely physical efficiency”. In secondary poverty, the income “would be sufficient for the maintenance of merely physical efficiency were it not that some portion of it is absorbed by some other expenditure.” Even with these rigorous criteria he found that 9.9% of the population was in primary poverty and a further 17.9% in secondary.[2]
Absolute and comparative poverty
More recent definitions tend to use the terms absolute and comparative poverty. Absolute is in line with Rowntree's primary poverty, but comparative poverty is usually expressed in terms of ability to play a part in the society in which a person lives. Comparative poverty will thus vary from one country to another.[3] The difficulty of definition is illustrated by the fact that a recession can actually reduce "poverty".
Causes of poverty
The causes of poverty most often considered are:
- Character defects
- An established “culture of poverty”, with low expectations handed down from one generation to another
- Unemployment
- Irregular employment, and/or low pay
- Position in the life cycle (see below) and household size
- Disability
- Structural inequality, both within countries and between countries. (R H Tawney: “What thoughtful rich people call the problem of poverty, thoughtful poor people call with equal justice a problem of riches”)[4]
As noted above, most of these, or the extent to which they can be, or should be changed, are matters of heated controversy.
- ↑ Alcock, P. Understanding poverty. Macmillan. 1997. ch 1.
- ↑ Harris, B. The origins of the British welfare state. Palgrave Macmillan. 2004. Also, Oxford Dictionary of National Biography.
- ↑ Alcock, Pt II
- ↑ Alcock, Preface to 1st edition and pt III.
